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Effects of supplementation with omega 3 long-chain polyunsaturated fatty acids on retinal and cortical development in premature infants.

Deficiency of omega 3 long-chain polyunsaturated fatty acids (LCPUFAs) in vertebrates produces subtle adverse effects on visual and neural function. Preterm infants 1) are deprived of vital intrauterine fat accretion during late pregnancy, 2) must rely solely on formula for fatty acid supplies if not breastfed, and 3) may have limited postnatal desaturase activity. In a study to evaluate the necessity of dietary omega 3 LCPUFAs, preterm infants were fed human milk, corn-oil-based formula (omega 3 fatty acid deficient), soy-oil-based formula (rich in precursor fatty acids), or marine-oil-supplemented formula (containing docosahexaenoic acid). At 36 and 57 wk postconception, the LCPUFA profiles in red blood cell lipids were nearly equivalent in the human-milk and marine-oil groups whereas the corn-oil group had markedly lower values for omega 3 fatty acids. Rod photoreceptor function was significantly less mature in the corn-oil group compared with the human-milk and marine-oil-enriched groups in early postnatal development (36 wk). The corn-oil group also had impaired visual acuity at both 36 and 57 wk. The potential benefit of omega 3 LCPUFA-enriched full-term formula is discussed. The study supports a role for omega 3 LCPUFAs as required nutrients for the optimal maturation of visual and cortical function in preterm infants.

Breast Feeding↗

Blood coagulation factor XIII contributes to the development of traction retinal detachment.

The blood coagulation factor XIII catalyzes the crosslinking of fibrin monomers at the end of the coagulation cascade. Additional functions are the enzymatic coupling of fibrinectin to itself, fibrin, and collagen. We located the two subunits of factor XIII in 20 surgically obtained periretinal membranes, using double label immunofluorescence microscopy. Both subunits of factor XIII could be detected in all specimens. The positive staining in all specimens examined prompted us to determine the source of factor XIII. The abundant fibroblastic cells did not contain factor XIII. Macrophages, half of which stained for the alpha-subunit of factor XIII could not account for the presence of factor XIII because these cells were not present in all specimens, and did not stain for the beta-subunit. Factor XIII is probably derived from the exudation of plasma and platelets through disrupted blood-ocular barriers. This is confirmed by the detection of both subunits in vitreous aspirates from patients with proliferative intraocular disorders (n = 15) by Western blotting.

Antibodies, Monoclonal↗

Is granuloma annulare related to intermediate uveitis with retinal vasculitis?

AIM: To report on eight patients with severe idiopathic intermediate uveitis (IU) and granuloma annulare (GA), a self limiting cutaneous condition of unknown aetiology. METHODS: Retrospective case series. Clinical ophthalmic and dermatological data were studied and fluorescein angiography and skin biopsies were reviewed. RESULTS: All patients with idiopathic IU had similar ocular features (eight with vitritis, seven with retinal vasculitis) and developed complications such as cystoid macular oedema (n=5), cataract (n=4), and glaucoma (n=3). Systemic diseases were not found, but a localised type of GA was observed in all. CONCLUSION: Seven out of eight patients with IU and GA developed severe retinal vasculitis. Further studies are needed for a better understanding of this association, a common pathogenesis, and its eventual clinical consequences.

Adolescent↗

Does light stimulus at eye opening of the developing rat influence retinal expression of GTP-binding protein (G(0))?

We previously hypothesized that light stimulus at eye opening of rats on postnatal days (P) 13 or 14 has an effect on the expression of GTP-binding proteins (G(0) in the retina) because the concentration of G(0) alpha increased rapidly between P10 and P15. This hypothesis was also supported by the findings that the distribution of G(0) alpha in the retina was almost the same as that of adult rats between P10 and P15. In this study, pregnant rats were kept in a dark room after vaginal plugs were identified; they gave birth to their pups in the dark, and their pups were reared by their mothers in the dark. The postnatal rats were sacrificed at P10, P15, P18, P22, P24, P27, and P30. Their retinas were investigated immunochemically and immunohistochemically, using G(0) alpha antibody, and these results were compared with those of the rat pups reared normally. Only G(0) alpha immunoreactivity in the inner nuclear layer of rats reared in the dark room was weaker than in the controls; the distribution of G(0) alpha in the retina did not change, as compared with pups reared in normal conditions. In addition, in pups reared in the dark, G(0) alpha increased rapidly from P10 to P15. However, the concentration of G(0) alpha in the retina of rat pups reared in the dark was significantly low at P22 (p < 0.01) and P30 (p < 0.05), as compared with pups reared in normal conditions. Although the function of G(0) in the retina may have something to do with the light stimulus after eye opening, it appeared that the expression of G(0) was not influenced by light stimulus at eye opening.

Animals↗

Immunohistochemical markers in full-thickness embryonic rabbit retinal transplants.

PURPOSE: To examine immunohistochemical markers in straight, well-laminated retinal transplants with special attention paid to the interphotoreceptor matrix, the Müller cells and the ganglion cells as these three retinal components have been abnormal in transplants produced by previous methods. METHODS: Nine rabbits underwent subretinal transplantation of a complete full-thickness embryonic neuroretina. After 31 or 49 days, the transplants were stained for light microscopy and processed for immunohistochemistry. RESULTS: Six of 9 eyes contained transplants with straight, well-laminated regions with all light-microscopic characteristics of a normal retina. In the outer segment region, the expression of peanut agglutinin showed segmental labeling of cone domains in the interphotoreceptor matrix, and interphotoreceptor retinoid binding protein immunoreactivity was found. Glial fibrillary acidic protein and vimentin immunoreactivity revealed normal Müller cell morphology. In 3 transplants the AB5-antibody-labeled ganglion cells in the ganglion cell layer and all transplants contained nerve fibers in the nerve fiber layer labeled by an antibody against neurofilament of 160 kD. The latter also labeled fibers connecting the transplant with the host. CONCLUSIONS: Full-thickness embryonic retinal transplants develop the normal retinal appearance and display several of the retinal components necessary for normal function which are not found in transplants produced by previous methods.

Animals↗

Monocarboxylate transporter expression remains unchanged during the development of diabetic retinal neuropathy in the rat.

PURPOSE: To determine the effect of diabetes on monocarboxylate transporter (MCT) expression in the rat retina. METHODS: Diabetes was induced in Wistar rats by a single intraperitoneal injection of streptozotocin (62.5 mg/kg). Rats were killed after 10 weeks, and the retinal levels of PKCalpha, bFGF, glial fibrillary acidic protein (GFAP), caspase-3, and MCT1, -2, and -4 were assessed with immunoblot analysis and RT-PCR. Hippocampal samples were used as a comparison. In other animals, the retinas were processed histologically and sections stained for the breakdown of DNA (TUNEL procedure) and for the distribution of MCT1, -2, and -4. RESULTS: Diabetic rats exhibited cataract formation, elevated blood glucose levels, and polydipsia. Retinal levels and distribution of MCT1, 2, and -4 were similar in the diabetic and age-matched control groups; however, the early retinopathy markers bFGF and PKCalpha were significantly elevated in the diabetic retinas but not in the hippocampal samples. ERG recordings showed decreased oscillatory potentials in the diabetic group, and TUNEL staining was most evident in the photoreceptor layer. Activated caspase-3 levels were elevated in the diabetic retina. CONCLUSIONS: The expression of retinal MCT1, -2, and -4 is unaffected after 10 weeks of diabetes in rats. It appears unlikely that diabetic retinal neuropathy is a result of a hyperglycemic induction of altered MCT expression.

Animals↗

Development of pressurized retinal resistance-sized arteriolar preparation with special reference to acetylcholine-induced nitric-oxide-mediated vasodilatation.

We examined the responses of pressurized bovine retinal functional arterioles (97-185 microm in diameter and approximately 3 mm long) to vasoactive substances and the mode of action of acetylcholine (ACh) on the pressurized arterioles. The retinal arterioles were cannulated at both ends with glass micropipettes and perfused at a constant pressure of 60 mmHg. Vasoconstrictions of the retinal arterioles were induced by prostaglandin F(2 alpha) (PG F(2 alpha)), U46,619, noradrenaline (NA), and 5-hydroxytryptamine (5-HT) in a dose-dependent manner. The decreasing order of potency (pD(2) value) in the constrictive responses was as follows: 5-HT = U46,619 > NA > PG F(2 alpha). On the other hand, sodium nitroprusside (SNP), isocarbacyclin (a stable prostaglandin I(2) analog), ACh, and isoproterenol (ISP) caused dose-dependent vasodilatation in the pressurized retinal arterioles preconstricted with high-potassium solution (40 mM K+). The decreasing order of potency in the vasodilative responses was as follows: isocarbacyclin > SNP > ACh. The ACh-induced vasodilatation was suppressed significantly by pretreatment with N omega-nitro-L-arginine methyl ester (L-NAME) (3 x 10(-5) M). A treatment with L-arginine (10(-3) M) in the presence of 3 x 10(-5) M L-NAME reversed completely the L-NAME-induced reduction of the vasodilatation. These results suggest that ACh causes the production and release of endogenous nitric oxide or its related compounds, which results in vasodilatation of the pressurized bovine retinal functional arterioles.

Acetylcholine↗

Adaptation to macular scotomas in persons with low vision.

Persons with scotomas in their central 20 degrees of vision often do not notice these blind spots within their visual field and have visual performance difficulties far exceeding what would be expected from standard vision tests. Before persons with macular scotomas can be assisted to optimally use their remaining vision for a better quality of life, more must be known about how the visual system adapts to a macular scotoma. Important issues include spatial and temporal characteristics of perceptual completion and metamorphopsia, development of preferred retinal loci for fixation and visual search, and dynamics of the preferred retinal locus development in terms of the changes in the eye movement system. With a full understanding of the visual system's adaptation to macular scotomas, new low vision devices and training techniques can be proposed to promote independence in activities of daily living for the person with low vision.

Activities of Daily Living↗

New insight into the functional role of acetylcholine in developing embryonic rat retinal neurons.

PURPOSE: To examine the effects of acetylcholine (ACh) on glutamate-induced neurotoxicity in embryonic rat retinal neurons. METHODS: Primary cultures were obtained from rat retinas at embryonic days 17 to 19. Cultured cells were exposed to glutamate for 10 minutes, followed by incubation in glutamate-free medium for 1 hour. Drugs were added to the incubation medium for 1 to 24 hours until immediately before glutamate exposure and were removed from culture medium during glutamate exposure and the postincubation period. The neurotoxic effects on retinal cultures were quantitatively assessed by the trypan blue exclusion method. RESULTS: Cell viability was markedly reduced by 10-minute exposure to 500 microM glutamate followed by a 1-hour incubation in glutamate-free medium. Incubating the cultures with 1 microM ACh for 12 hours before glutamate exposure reduced glutamate neurotoxicity. A similar effect was induced by application of carbachol (1 microM). The protective effect of ACh against glutamate neurotoxicity was inhibited by a nicotinic acetylcholine receptor (nAChR) antagonist, mecamylamine (0.5 microM), whereas a muscarinic acetylcholine receptor (mAChR) antagonist, atropine (0.5 microM) did not affect ACh-induced protection. In addition, a similar protection was induced by application of nicotine (1 microM), but not by muscarine (1 microM). Pretreatment with nicotine induced a protective effect in a time-dependent manner, ranging from 1 to 12 hours. Pretreatment with nicotine at concentrations ranging from 0.001 to 1 microM induced dose-dependent protection against glutamate neurotoxicity. Furthermore, the protective action of nicotine was inhibited by simultaneous application of dopamine D1 receptor antagonist, SCH23390 (1 microM), with nicotine, whereas a dopamine D2 receptor antagonist, domperidone (1 microM), did not affect nicotine-induced protection. CONCLUSIONS: These results suggest that pretreatment of cultured rat retinal neurons with ACh or the nAChR agonists, nicotine and carbachol, has a protective action against glutamate neurotoxicity through nAChRs and that the dopamine release induced by nicotinic stimulation subsequently protects the retinal neurons by way of dopamine D1 receptors.

Acetylcholine↗

[Prenatal development of human retinal vessels].

Feeding of the retina, whose thickness does not exceed 130 mu km, is possible at the account of chriocapillary diffusion. Should this threshold be topped (approximately by the 3.5th prenatal month), it will result in a relative hypoxia of the uttermost internal strata of the retina, which induces the appearance of new feeding source, i.e. retinal vessels. First, dense cellular steaks of the sequential fusiform cells originating from the visual-stem depth located near the wall of a. hyaloidea emerge in the surface retinal strata. These cells (angioblasts) formed the peripapillary plexus, shaped as a vascular pattern, and represented a non-lumenized prototype, or matrix, of a future capillary network. Later, main arterioles emerged, in the outward direction from them, and after that venules took shape from the above network through a partial reduction of vessels and a redistribution of blood circulation. The second deep capillary stratum was formed rather through a prolongation and "sagging" of the surface capillary loops than through gemmation; it is common for the entire retina and, unlike the surface stratum, is not divided by main arterioles into adjoining segments. By the 8th fetal-life month the evolution of the retinal bloodstream is not entirely completed, though it resembles, to a great extent, a definitive one.

Arterioles↗

Surgical management of non-metallic and non-magnetic metallic intraocular foreign bodies.

BACKGROUND AND OBJECTIVE: To identify clinical features and evaluate outcomes of vitreoretinal surgery in eyes with retained non-metallic and non-magnetic metallic intraocular foreign bodies (IOFBs). PATIENTS AND METHODS: Retrospective chart review. Thirty-two eyes (28 patients) with non-metallic and non-magnetic metallic IOFBs underwent removal of IOFBs with intraocular forceps, either via the pars plana in 30 eyes (93.9%) or a limbal approach in 2 eyes (6.25%). The main outcome measures were postoperative visual acuity, rate of retinal break formation, development of retinal detachment, and type of IOFB. RESULTS: IOFBs were non-metallic in 22 eyes (68.7%) and non-magnetic metallic in 10 eyes (31.1%). The average follow-up period was 7.5 months. Overall, final visual acuity was 20/40 or better in 10 eyes (31.1%) and 5/200 to 20/50 in 10 eyes (31.1%). A higher incidence of retinal break formation posterior to the sclerotomy was seen with glass IOFBs (P = .02). Retinal detachment was observed preoperatively in 4 eyes (12.5%) and postoperatively in 2 eyes (6.25%). CONCLUSION: Final visual outcome was independent of size and type of IOFB. Pars plana extractions may be associated with a higher rate of retinal break formation and subsequent retinal detachment, particularly with glass IOFBs.

Adolescent↗